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PowerPoint Presentation for
Biopsychology, 8th Edition
by John P.J. Pinel
Prepared by Jeffrey W. Grimm
Western Washington University
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Inc. All rights reserved.
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Chapter 9
Development of the Nervous
System
From Fertilized Egg to You
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Neurodevelopment
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Neural development – an ongoing process;
the nervous system is plastic
A complex process
Experience plays a key role
Dire consequences when something goes
wrong
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The Case of Genie
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At age 13, Genie weighed 62 pounds and
could not chew solid food
Beaten, starved, restrained, kept in a dark
room, denied normal human interactions
Even with special care and training after
rescue, her behavior never became normal
Case of Genie illustrates the impact of severe
deprivation on development
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Phases of Development
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Ovum + sperm = zygote
Developing neurons accomplish these things
in five phases
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Induction of the neural plate
Neural proliferation
Migration and aggregation
Axon growth and synapse formation
Neuron death and synapse rearrangement
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Induction of the Neural Plate
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A patch of tissue on the dorsal surface of the
embryo becomes the neural plate
Development induced by chemical signals from
the mesoderm (the “organizer”)
Visible three weeks after conception
Three layers of embryonic cells
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Ectoderm (outermost)
Mesoderm (middle)
Endoderm (innermost)
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Induction of the Neural Plate
Continued
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Neural plate cells are often referred to as
embryonic stem cells
Have unlimited capacity for self renewal
Can become any kind of mature cell
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Totipotent – earliest cells have the ability to
become any type of body cell
Multipotent – with development, neural plate
cells are limited to becoming one of the range of
mature nervous system cells
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FIGURE 9.1 How the neural plate
develops into the neural tube during
the third and fourth weeks of human
embryological development.
(Adapted from Cowan, 1979.)
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Neural Proliferation
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Neural plate folds to form the neural groove,
which then fuses to form the neural tube
Inside will be the cerebral ventricles and neural
tube
Neural tube cells proliferate in species-specific
ways: three swellings at the anterior end in
humans will become the forebrain, midbrain,
and hindbrain
Proliferation is chemically guided by the
organizer areas – the roof plate and the floor
plate
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Migration
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Once cells have been created through cell
division in the ventricular zone of the
neural tube, they migrate
Migrating cells are immature, lacking
axons and dendrites
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Migration Continued
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Two types of neural tube migration
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Two methods of migration
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Radial migration (moving out) – usually by moving
along radial glial cells
Tangential migration (moving up)
Somal – an extension develops that leads
migration, cell body follows
Glial-mediated migration – cell moves along a
radial glial network
Most cells engage in both types of migration
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FIGURE 9.2 The two types of
neural migration: radial
migration and tangential
migration.
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FIGURE 9.3 Two methods by which cells
migrate in the develping neural tube: somal
translocation and glia-mediated migration.
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Neural Crest
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A structure dorsal to the neural tube and
formed from neural tube cells
Develops into the cells of the peripheral
nervous system
Cells migrate long distances
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Aggregation
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After migration, cells align themselves
with others cells and form structures
Cell-adhesion molecules (CAMs)
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Aid both migration and aggregation
CAMs recognize and adhere to molecules
Gap junctions pass cytoplasm between
cells
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Prevalent in brain development
May play a role in aggregation and other
processes
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Axon Growth and Synapse
Formation
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Once migration is complete and structures
have formed (aggregation), axons and
dendrites begin to grow
Growth cone – at the growing tip of each
extension, extends and retracts filopodia as
if finding its way
Chemoaffinity hypothesis – postsynaptic
targets release a chemical that guides
axonal growth, but this does not explain the
often circuitous routes often observed
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FIGURE 9.5 Sperry’s classic study
of eye rotation and regeneration.
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Axon Growth and Synapse
Formation Continued
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Mechanisms underlying axonal growth are
the same across species
A series of chemical signals exist along the
way – attracting and repelling
Such guidance molecules are often
released by glia
Adjacent growing axons also provide
signals
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Axon Growth and Synapse
Formation Continued
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Pioneer growth cones – the first to travel a
route, interact with guidance molecules
Fasciculation – the tendency of
developing axons to grow along the paths
established by preceding axons
Topographic gradient hypothesis – seeks
to explain topographic maps
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FIGURE 9.7 The topographic gradient
hypothesis. Gradients of ephrin-A and
ephrin-B on the developing retina (see
McLaughlin, Hindges, & O’Leary, 2003).
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Synapse Formation
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Formation of new synapses
Depends on the presence of glial cells –
especially astrocytes
High levels of cholesterol are needed –
supplied by astrocytes
Chemical signal exchange between pre- and
postsynaptic neurons is needed
A variety of signals act on developing
neurons
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Neuron Death and Synapse
Rearrangement
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~50% more neurons than are needed are
produced – death is normal
Neurons die due to failure to compete for
chemicals provided by targets
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The more targets, the fewer cell deaths
Destroying some cells increases survival rate
of remaining cells
Increasing number of innervating axons
decreases the proportion that survives
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Life-Preserving Chemicals
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Neurotrophins – promote growth and
survival, guide axons, stimulate
synaptogenesis
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Nerve growth factor (NGF)
Both passive cell death (necrosis) and
active cell death (apoptosis)
Apoptosis is safer than necrosis – does
not promote inflammation
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Synapse Rearrangement
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Neurons that fail to establish correct
connections are particularly likely to die
Space left after apoptosis is filled by
sprouting axon terminals of surviving
neurons
Ultimately leads to increased selectivity of
transmission
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FIGURE 9.8 The effect
of neuron death and
synapse rearrangement
on the selectivity of
synaptic transmission.
The synaptic contacts
of each axon become
focused on a smaller
number of cells
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Postnatal Cerebral
Development in Human Infants
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Postnatal growth is a consequence of
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Synaptogenesis
Myelination – sensory areas and then motor
areas. Myelination of prefrontal cortex
continues into adolescence
Increased dendritic branches
Overproduction of synapses may underlie
the greater plasticity of the young brain
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Development of the Prefrontal
Cortex
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Believed to underlie age-related changes
in cognitive function
No single theory explains the function of
this area
Prefrontal cortex plays a role in working
memory, planning and carrying out
sequences of actions, and inhibiting
inappropriate responses
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Effects of Experience on the
Early Development,
Maintenance, and Reorganization
of Neural Circuits
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Permissive experiences: those that are
necessary for information in genetic
programs to be manifested
Instructive experiences: those that
contribute to the direction of development
Effects of experience on development are
time-dependent
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Critical period
Sensitive period
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Early Studies of Experience
and Neurodevelopment
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Early visual deprivation
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Fewer synapses and dendritic spines in primary
visual cortex
Deficits in depth and pattern vision
Enriched environment
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Thicker cortexes
Greater dendritic development
More synapses per neuron
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Competitive Nature of
Experience and
Neurodevelopment
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Ocular Dominance Columns example:
Monocular deprivation changes the pattern
of synaptic input into layer IV of V1 (but
not binocular deprivation)
Altered exposure during a sensitive period
leads to reorganization
Active motor neurons take precedence
over inactive ones
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FIGURE 9.10 The effect of a few days of early monocular
deprivation on the structure of axons projecting from
the lateral geniculate nucleus into layer IV of the
primary visual cortex. Axons carrying information from
the deprived eye displayed substantially less branching.
(Adapted from Antonini & Stryker, 1993.)
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Effects of Experience on
Topographic Sensory Cortex
Maps
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Cross-modal rewiring experiments demonstrate the plasticity of sensory cortexes – with
visual input, the auditory cortex can see
Change input, change cortical topography –
shifted auditory map in prism-exposed owls
Early music training influences the
organization of human auditory cortex – fMRI
studies
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Experience Fine-Tunes
Neurodevelopment
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Neural activity regulates the expression of
genes that direct the synthesis of CAMs
Neural activity influences the release of
neurotrophins
Some neural circuits are spontaneously
active and this activity is needed for
normal development
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Neuroplasticity in Adults
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The mature brain changes and adapts
Neurogenesis (growth of new neurons)
seen in olfactory bulbs and
hippocampuses of adult mammals – adult
neural stem cells created in the ependymal
layer lining in ventricles and adjacent
tissues
enriched environments and exercise can
promote neurogenesis
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FIGURE 9.11 Adult neurogenesis.
(Courtesy of Carl Ernst and Brian
Christie, Department of
Psychology, University of British
Columbia.)
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Effects of Experience on the
Reorganization of the Adult
Cortex
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Tinnitus (ringing in the ears) – produces
major reorganization of primary auditory
cortex
Adult musicians who play instruments
fingered by left hand have an enlarged
representation of the hand in the right
somatosensory cortex
Skill training leads to reorganization of
motor cortex
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Disorders of
Neurodevelopment: Autism
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Three core symptoms
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Reduced ability to interpret emotions and
intentions
Reduced capacity for social interaction
Preoccupation with a single subject or activity
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Disorders of
Neurodevelopment: Autism
Continued
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Intensive behavioral therapy may improve
function
Heterogenous – level of brain damage and
dysfunction varies
Often considered a spectrum disorder
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Autism spectrum disorders
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Asperger’s syndrome
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Mild autism spectrum disorder in which cognitive and
linguistic functions are well preserved
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Disorders of
Neurodevelopment: Autism
Continued
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Incidence: 6.6 per 1,000 births (or 1 in 166)
80% males, 60% mentally retarded, 35% epileptic,
25% have little or no language ability
Most have some abilities preserved – rote memory,
jigsaw puzzles, musical ability, artistic ability
Autistic Savants – intellectually handicapped
individuals who display specific cognitive or artistic
abilities
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~1/10 autistic individuals display savant abilities
Perhaps a consequence of compensatory functional
improvement in one area following damage to another
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Genetic Basis of Autism
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Siblings of the autistic have a 5% chance
of being autistic
60% concordance rate for monozygotic
twins
Several genes interacting with the
environment
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Neural Mechanisms of Autism
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Understanding of brain structures involved
in autism is still limited, so far implicated:
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Cerebellum
Amygdala
Frontal cortex
Two lines of research on cortical
involvement in autism:
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Abnormal response to faces in autistic patients
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Spend less time than non-autistic subjects looking
at faces, especially eyes
Low fMRI activity in fusiform face area
Possibly deficient in mirror neuron function
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Disorders of
Neurodevelopment:
Williams Syndrome
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1 in every 7,500 births
Mental retardation and an uneven pattern of
abilities and disabilities
Sociable, empathetic, and talkative – exhibit
language skills, music skills, and an enhanced
ability to recognize faces
Profound impairments in spatial cognition
Usually have heart disorders associated with a
mutation in a gene on chromosome 7 – the gene
(and others) is absent in 95% of those with
Williams
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Disorders of
Neurodevelopment:
Williams Syndrome Continued
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Evidence for a role of chromosome 7 (as in
autism)
General thinning of cortex at juncture of
occipital and parietal lobes, and at the
orbitofrontal cortex
“Elfin” appearance – short, small upturned
noses, oval ears, broad mouths
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FIGURE 9.13 Two areas of reduced cortical volume and
one area of increased cortical volume observed in
people with Williams syndrome. (See Meyer-Lindenberg
et al., 2006; Toga & Thompson, 2005.)
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